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Continuous cultivation of murine L cells infected with lymphocytic choriomeningitis virus strain Armstrong leads to production of L(Arm) cells, which produce a predominantly cell-associated attenuated variant, the L(Arm) virus. The relatively few infectious particles that are released have lost the ability to form plaques on L cells and to cause illness in mice even if inoculated intracerebrally. Based on equal protein M(r)s, antigenicity and protein kinase activity, essentially identical results were obtained for the purified Armstrong and L(Arm) viruses. There was also no difference in production and release of particles with the potential to cause homologous interference. Such particles consisted of two types, one of which was highly susceptible to u.v.-irradiation, the other was highly resistant. In the case of the L(Arm) virus interfering particles, it appears that the u.v.-irradiation-susceptible forms represented infectious virus. Purified L(Arm) virus particles contained considerable quantities of subgenomic forms of (small) S- and (large) L-RNA and their complementary counterparts, which all appeared to be replicated autonomously in an unenriched manner.

During persistent infection of mouse L cells with strain Armstrong lymphocytic choriomeningitis virus, the latter undergoes characteristic changes, including loss of mouse pathogenicity and failure to form plaques on cultivated cells. We call this virus L(Arm) and have analyzed transcription and translation of its S-RNA, which codes for the viral nucleoprotein (NP) and the glycoprotein precursor (GP-C). In L(Arm) virus-infected L cells, S-RNA and genomic-sized viral complementary S-RNA (VC-S-RNA) were detected and, in addition, considerable quantities of shortened molecules of either species. The cells' content of NP was high, but they contained little GP-C; instead, a viral glycoprotein with MW 65,000 was present. We propose a hypothesis in which it is assumed that along the VC-S-RNA there is more than one recognition site for the viral RNA-dependent RNA polymerase, which leads to the generation of truncated forms of S-RNA, VC-S-RNA, and mRNA for GP-C; this, in turn, results in relative overproduction of NP and relative underproduction of GP-C as well as the emergence of a new form of viral glycoprotein.